An endophytic fungus, Piriformospora indica, enhances drought tolerance of trifoliate orange by modulating the antioxidant defense system and composition of fatty acids.

A cultivable endophytic fungus, Piriformospora indica, improves growth and enhances stress tolerance of host plants, but the underlying mechanisms remain unknown. We hypothesized that P. indica enhanced the drought tolerance of the host by regulating the antioxidant defense system and composition of fatty acids. Trifoliate orange (Poncirus trifoliata) seedlings were inoculated with P. indica under ample water and drought stress to analyze the change in plant growth, reactive oxygen species (ROS) levels, antioxidant enzyme activities, non-enzymatic antioxidant concentrations, fatty acid compositions, and expressions of both antioxidant enzyme genes and fatty acid desaturase (FAD) genes. The 9-week soil water deficit significantly increased the colonization of P. indica to roots, and P. indica promoted the increase of shoot biomass under drought. Soil drought triggered an elevation of hydrogen peroxide in roots, while the inoculated plants had lower levels of ROS (hydrogen peroxide and superoxide anion radicals) and lower degree of membrane lipid peroxidation (based on malondialdehyde levels) under drought. Drought treatment also elevated ascorbic acid and glutathione concentrations, and the elevation was further amplified after P. indica inoculation. Inoculated plants under drought also recorded significantly higher iron-superoxide dismutase (Fe-SOD), manganese-superoxide dismutase (Mn-SOD), peroxidases, catalase, glutathione reductase and ascorbate peroxidase activities, accompanied by up-regulation of PtFe-SOD and PtCu/Zn-SOD expressions. Inoculation with P. indica significantly increased total saturated fatty acids (e.g., C6:0, C15:0, C16:0, C23:0 and C24:0) concentration and reduced total unsaturated fatty acids (e.g., C18:1N9C, C18:2N6, C18:3N3, C18:1N12 and C19:1N9T) concentrations, leading to a decrease in the unsaturation index of fatty acids, which may be associated with the up-regulation of PtFAD2 and PtFAD6 and down-regulation of PtΔ9. It was concluded that the colonization of P. indica can activate enzyme and non-enzyme defense systems and regulate the composition of fatty acids under drought, thus alleviating the oxidative damage to the host caused by drought.

Loss of RTN3 phenocopies chronic kidney disease and results in activation of the IGF2-JAK2 pathway in proximal tubular epithelial cells.

Reticulon 3 (RTN3) is an endoplasmic reticulum protein that has previously been shown to play roles in neurodegenerative diseases, but little is known about its function in the kidneys. The aim of the present study was to clarify the roles of RTN3 in chronic kidney disease (CKD) and kidney fibrosis. In this study, RTN3 levels were measured in kidney tissues from healthy controls and CKD or kidney fibrosis patients. An RTN3-null mouse model was generated to explore the pathophysiological roles of RTN3 in the kidneys. The underlying mechanisms were studied in primary proximal tubular epithelial cells and HEK293 cells in vitro. The results showed that (1) a reduction in RTN3 in mice induces CKD and kidney fibrosis; (2) decreased RTN3 expression is found in patients with CKD; (3) RTN3 plays critical roles in regulating collagen biosynthesis and mitochondrial function; and (4) mechanistically, RTN3 regulates these phenotypes by interacting with GC-Rich Promoter Binding Protein 1 (GPBP1), which activates the IGF2-JAK2-STAT3 pathway. Our study indicates that RTN3 might play crucial roles in CKD and kidney fibrosis and that a reduction in RTN3 in the kidneys might be a risk factor for CKD and kidney fibrosis.